The Crohnie

Another piece of research which establishes the anti-paratuberculosis antibiotic activity of molecules which are currently thought to have an immuno-suppressant effect in Crohn’s Disease.

http://www.paratuberculosis.org/pubs/proc9/abst185f_o4.htm

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BACKGROUND:

We have shown that the “immuno-modulators” methotrexate and 6-MP and the “anti-inflammatory” 5-ASA inhibit MAP growth (www.PLoSONE.org) and concluded that their most plausible mechanism of action in several idiopathic diseases is as antiMAP antibiotics. Thalidomide is an “immunomodulator” used in multiple “auto-immune” and “inflammatory” diseases and the mycobacterial diseases leprosy and tuberculosis. We now test the hypothesis that thalidomide inhibits MAP growth.

METHODS

Thalidomide (+-) and (+) and (-) and its two components, phthalimide and 1-hydroxy 2,6 piperidine dione (HPD) were evaluated in culture of two strains each of MAP (ATCC 19698 [bovine] & Dominic [human]) and M. avium subspecies avium (ATCC 25291 & 101.) We used a radiometric (14CO2 Bactec(R)) detection system. Inhibition is indicated by “percent decrease in cumulative Growth Index” (%-DcGI) from control.

RESULTS:

Phthalimide has no dose dependent inhibition on any strain. There was no dose dependent inhibition on either M. avium strain with thalidomide or its components. With the two MAP strains, there is dose dependent inhibition with thalidomide (+1); Dominic (31%-DcGI) and ATCC 19698 (26%-DcGI) at 64microg/ml. Thalidomide (+) is more inhibitory than (-). HPD is, on a weight for weight basis, the most inhibitory agent evaluated; Dominic (46%-DcGI) and ATCC 19698 (44%-DcGI at 64microg/ml)

CONCLUSIONS:

We show in vitro heretofore-undescribed inhibition of MAP growth by racaemic thalidomide. Thalidomide (+) is more potent than (-). Of thalidomide’s two moieties, phthalimide has no antiMAP activity and HPD is the active component in inhibiting MAP growth. We suggest that since 1942, initially with 5-ASA, the medical profession has unknowingly been treating MAP infections. These data are compatible with our concern that MAP is zoonotic. We conclude that all idiopathic “autoimmune” and “inflammatory” diseases, empirically treated with medications that we show are active against MAP, should now be evaluated for MAP as the etiological agent.

Behcet’s disease is a disease that can be confused with Crohn’s Disease, since it exhibits a spectrum of symptoms which overlaps with the spectrum of symptoms displayed in CD.

Check the references below.

The bit I find most interesting is the reliance on human opinion and experience to differentiate between the diseases. The reason for this is because we’re dealing with diseases that are classified by the damage that results from having them, not by what causes them.

Personal opinion: The vast majority of “autoimmune” diseases are caused by infections with one or more of a range of bacteria, and where the symptoms can be extremely similar.

Research into all of these diseases needs a fundamental shift in paradigm. Looking solely at the body, its reactions, and how those reactions result in tissue damage is incapable of delivering a cure.

Consider if you drove your car home every day along a road that was covered in shards of glass. When you get home, you see that you have flat tyres. You examine the car, you examine the tyres, you work out the weight distribution on the wheels, trying to imagine a situation where the car tyres “spontaneously” blow out. You spend a fortune, getting an army of “experts” to try to figure out why your tyres keep blowing out. They spend a fortune in money and time trying to figure the huge range of parameters that can affect the car, even going so far as to revisit the production process for the car, watching how it is constructed in the factory, and trying to discover the “design flaw” that results in the tyres spontaneously bursting.

And you still keep getting flat tyres everyday.

Until you look at the surface of the road you’re driving on, and realise that it’s covered in glass, which damages your rubber tyres, you’re not going to have the faintest clue as to why your tyres are flat everyday.

1. An unusual presentation of Behcet’s disease: intestinal perforation.
Pirildar T, Keser G, Tunc E, Alkanat M, Tuncyurek M, Doganavsargil E.
http://www.ncbi.nlm.nih.gov/pubmed/11254244

2. Crohn’s disease with Behcet’s syndrome like appearance: a case report.
Kallinowski B, Noldge G, Stiehl A.
http://www.ncbi.nlm.nih.gov/pubmed/7886973

3. Pathology of chronic inflammatory bowel disease in children.
Domizio P.
http://www.ncbi.nlm.nih.gov/pubmed/8003743

4. Bechet’s colitis: a differential diagnosis in inflammations of the large intestine.
Kyle SM, Yeong ML, Isbister WH, Clark SP.
http://www.ncbi.nlm.nih.gov/pubmed/1859318

5. Prerequisites for therapy of inflammatory bowel diseases. Pathophysiology–symptomatology–diagnosis
Haag K, Scholmerich J.
http://www.ncbi.nlm.nih.gov/pubmed/1855748

I came across an interesting article, published by the American College of Physicians. It discusses the topic of “autoimmune” diseases, and how many diseases originally thought to be autoimmune diseases are really infectious diseases. IBD is discussed in brief, with reference to both mycobacterial infection and measles infection.

You can read it at

http://www.acponline.org/journals/annals/15nov96/infdis.htm

It provides a good overview of medical opinions on many illnesses are changing.